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Doomsday 2: No One Knows When the Next Plague Will Come, Only That It Will

June 17, 2014
by Glen Martin
A crowded drawing of people Image source: Andrew Archer

The first confirmed victim was a Vietnamese butcher in Láo Cai. He collapsed suddenly while chopping up pork ribs in his outdoor stall, and died within hours.

Family members said he had been feeling ill for several days,had been coughing constantly for two, but insisted on working. It was a point of pride with him, they said. After several days, they too were stricken, and most died. Then people who had bought meat from the butcher sickened and expired. Then their neighbors succumbed. Then people across the river, down the road, over the next mountain.

The epidemic raged through Láo Cai, and also the neighboring towns of Cao Bang and Thái Nguyên. Before any effective containment strategy could be devised, it had spread to Nanning and Kunming in China, and then it reached Macao—and finally, Hong Kong. And from there, it literally took flight around the world. Within weeks, people were coughing, collapsing, and dying in San Francisco, Sydney, London, and São Paolo.

Virologists and microbiologists analyzed the responsible pathogen and found it was a coronavirus, kin to the SARS microbe that briefly induced global panic before it was contained in 2003. But this coronavirus contained RNA from Influenza C, a virus that infects pigs as well as humans. This new hybrid bug had probably originated on a small farm, incubating in both the farmer and his swine. When the pigs went to market, the new coronavirus was poised to make its debut.

It was stunningly virulent. The “Spanish flu” epidemic of 1918 had a 2 percent direct mortality rate (though many more died from secondary bacterial pneumonia). The 2003 SARS outbreak had a general mortality rate of more than 10 percent, climbing to 50 percent in people middle-aged or older. But this new pathogen had a general mortality rate of 31 percent, hitting 67 percent in people 60 years or older. Normally, virulence works against the rapid spread of a virus; people who are violently ill generally aren’t effective at disease transmission, because they quickly become too sick to walk around and shed microbes in public venues. But this coronavirus had a long incubation period. Many people harbored “subclinical” infections for days or even weeks; they were highly infectious and ambulatory prior to developing full-blown, incapacitating symptoms. In short, the disease was widely dispersed before anyone recognized its existence.

The medical community named the new plague Massive Acute Respiratory Syndrome, or MARS. But as it gained momentum and began killing millions, then tens of millions, it gained a popular, and more sinister moniker: Reaper.

The above scenario is extreme, but is by no means impossible—or even unlikely. In fact, the emergence of pathogens capable of causing global pandemics that kill millions, if not billions, of people is inevitable.

It will be nothing new. We have evolved with viruses and bacteria, many of them lethal. Pandemics have accompanied us from the caves to the skyscrapers, shaping who we are genetically and socially. The bubonic plague, caused by the bacterium Y. pestis, likely contributed to the fall of Rome: The so-called Justinianic Plague raged from the 6th to 8th centuries and killed about 100 million people in lands controlled by the Empire. Similarly, the Y. pestis–driven Black Death wiped out a third or more of Europe’s population in the 14th century and changed the genome of Continental people, selecting for certain genes involved in immune response. In short, most of the living things on the planet are microbiological. To a very real degree, we are mere hosts, living petri dishes for creatures inhabiting the microcosmic world. We cannot stop them. We can only accommodate and sometimes divert them. Moreover, the threat is and will remain imminent. We’ve recently dodged some very near bullets from the microcosmos.

“SARS—that was the big wake-up call,” said Tomás Aragón, an assistant adjunct professor of epidemiology at UC Berkeley’s School of Public Health. “It was completely unexpected. It had 11 percent overall mortality and 50 percent mortality in people over 50. We had no vaccine for it. It was incredibly scary.”

“No place on earth is more than a multi-hour jet flight from any­place else. That kind of com­plex­ity vastly in­creases our vul­ner­ab­il­ity. It al­lows for cas­cades of trans­mis­sion.”

Luckily, SARS’s virulence provided a certain edge to public health officials: It made the coronavirus easier to track and ultimately to contain. Also, noted Aragón, “We were fortunate in that it wasn’t extremely infectious. Those two factors—that it was easy to identify because the symptoms were so extreme and that it was relatively difficult to contract—made it possible to ultimately contain the outbreaks.” SARS racked up more than 8,000 cases and at least 775 deaths before it was stopped.

On the surface, then, the evidence suggests our modern world is a safer place than the Dark Ages or the Roman era, when pandemics killed millions. Yes and no. Detection and response capabilities are superior today, but when it comes to pandemics, one modern technology favors the pathogens: high-speed transportation.

“Everything considered, the modern world is a downside when it comes to disease control,” said Aragón. “Look at what the Spanish Flu epidemic did in 1918, when it was relatively difficult for people to get around. Within a year, it had infected people on every continent. And today, we’re a much more complex, connected, and interdependent society. No place on earth is more than a multi-hour jet flight from anyplace else. That kind of complexity vastly increases our vulnerability. It allows for cascades of transmission.”

While SARS didn’t blow up into a global pandemic, neither was it eliminated as a threat. It is widely assumed the coronavirus that caused it is merely quiescent, not extinct. And as of this writing, a related malady—Middle East Respiratory Syndrome, or MERS—has resulted in numerous fatalities in the Mideast, Europe, and North Africa, and two cases have been confirmed in North America. Like SARS, it is caused by a coronavirus, has a high mortality rate, and is difficult to transmit.

The basic trouble with viruses is their adaptability and their protean nature. They are highly adept at swapping genetic material, allowing them to exploit new opportunities for dispersion and propagation. This happens primarily through zoonosis: Viruses leap from one species to another, producing new variants at each step. Fruit bats, for example, may defecate in a hog pen on a Cambodian farm. The pigs ingest the bat feces. Viruses in the waste commingle with pig viruses, and the resultant microbe may then leap to the farmer who feeds the pigs, where it interacts with human viruses. Such viral “reassortment,” as microbiologists term it, can result in particularly virulent strains.

“Reassortment is the major worry,” said Aragón, “simply because you can get these abrupt and completely unexpected creations of new microbes with really lethal characteristics.

Of all the viruses that have the potential for becoming global “slate-cleaners,” no group is more feared than the African hemorrhagic fevers, specifically Ebola, Marburg, and Lassa. They appear zoonotic in origin, having likely jumped from monkeys and fruit bats to humans via the bush meat trade—wild game remains a preferred source of protein in West Africa, and is widely marketed and consumed.

They are without question horrifying diseases. The fevers they induce are extreme, and victims bleed subcutaneously and from the eyes and orifices. The mortality rates are jaw-dropping. In some Ebola outbreaks, the death rate reached 90 percent. Such outbreaks seem to be increasing in frequency and severity (or at least they’re more widely reported). As of this writing, a particularly stubborn Ebola epidemic in Guinea has claimed at least 150 lives, and public health officials have expressed concern it could spread beyond Africa.

That said, Ebola and similar viruses are relatively hard to contract, typically spreading by contact with body fluids. In West Africa—where most of the cases emerge—transmission is greatly augmented by cultural imperatives that require the washing of dead bodies before burial or cremation.

To make matters worse, these viruses can have relatively long incubation periods. Ebola can lurk in the human body for three or four weeks prior to manifesting, and infected people can spread it even in the asymptomatic phase. That’s a big problem, but an even bigger one could be reassortment: What happens if an Ebola virus and an influenza virus swap RNA? In other words, what if an Ebola variant emerges that can be spread like influenza or the common cold—through the inhalation of virus-contaminated aerosols released by coughing or sneezing?

“The fact is that we have many ‘pan­dem­ics’ go­ing on around the world in­volving drug-res­ist­ant bac­teria. Com­pared to vir­uses, bac­teria usu­ally don’t spread rap­idly, so they’re kind of slow-mo­tion pan­dem­ics. That doesn’t mean they’re not ser­i­ous.”

“It’s the nightmare scenario,” said Professor Arthur Reingold, the head of epidemiology of Berkeley’s School of Public Health. “How likely is it to happen? It’s one of those unknown unknowns. It’d be catastrophic if it did happen, but I consider it highly unlikely.”

Viruses are not the only concern; bacteria also constitute a major threat to public health. And it’s a threat that’s growing, in large part because the primary weapon in the anti-bacterial armamentarium—antibiotics—has been both misused and overused. Antibiotics have been tremendously effective in beating back a wide range of disease-inducing infections over the years, but that’s all they can do: Keep the bugs in check. They can’t eliminate them. Invariably, bacteria emerge that are resistant to specific drugs. And as the use of antibiotics has increased in human medicine, veterinary medicine—even in agriculture, where they are fed to livestock to maximize weight gains and minimize the infections inherent to factory farming—the bacterial realm in general has become more robust.

“Even common bacteria, bacteria that have been relatively easy to treat such as E. coli, are becoming increasingly resistant,” said Lee Riley, a professor of infectious diseases and epidemiology at Berkeley’s School of Public Health and the chair of the Division of Infectious Diseases and Vaccinology. “In Japan, you’re seeing more and more cases of ‘simple’ urinary tract infections (caused by E. coli) that can’t be dealt with on an outpatient basis. They have to go in for hospital treatment, often involving extended stays. That puts a tremendous burden on the public health system.”

Riley is particularly concerned about Costridium difficile, a gram-positive bacterium associated with intestinal infections that is developing resistance to a wide spectrum of antibiotics.

“It was once pretty much confined to hospitals, but it’s now appearing in the general community,” said Riley. “It’s a very tough microbe, and its impact mustn’t be underestimated. C. difficile–related colitis kills 14,000 people annually in the United States alone, and it’s not getting the attention it deserves. When an airplane crashes, it’s news. When there’s a flu epidemic and several hundred people die, it’s news. But for some reason, it’s not news when thousands of people die annually in car crashes. Nor is it news when people are hospitalized for bacterial infections and later die, even if it amounts to thousands of casualties a year.”

Tuberculosis presents similar challenges, observed Russell Vance, an associate professor of immunology and pathogenesis at Berkeley’s Department of Molecular and Cell Biology. Multi-drug-resistant TB, which is impervious to at least two of the antibiotics typically used to treat the disease, is now prevalent, accounting for about 500,000 new cases annually; about 150,000 people die from this variant a year. An even more tenacious TB bacillus has emerged that is extensively drug-resistant, but it is—so far, anyway—rare.

“Right now [resistant forms of TB] are largely confined to the developing world,” Vance said. “But to say ‘it’s not our problem’ would be a huge mistake. It’s a very expensive disease to treat. You have to maintain a rigorous course of antibiotics for months and months. If it became established in the U.S., it would be a public health disaster.”

“Here’s where the great un­cer­tain­ties lie. If you say you have the an­swers, you’re de­lu­sion­al. We know there will be pan­dem­ics. We don’t know when and how.”

Compounding the bacteria problem is the generally unregulated use of antibiotics in Asia, Africa and Latin America—especially the urban slums, Riley observes. There, powerful antibiotics are generally available over-the-counter. Many antibiotics have relatively narrow ranges of application, and, without physician oversight, are often mis-prescribed. Even when the prescription is on the mark, many patients fail to complete the full course of treatment. Both scenarios encourage the proliferation of drug-resistant bacteria.

“The fact is that we have many ‘pandemics’ going on around the world involving drug-resistant bacteria,” said Riley. “But compared to viruses, bacteria usually don’t spread rapidly, so they’re kind of slow-motion pandemics. That doesn’t mean they’re not serious.”

Riley further points out that viruses and bacteria often work in malign concert. Most of the people who died in the 1918 Spanish Flu pandemic didn’t perish directly from influenza. They died from bacteria-induced pneumonia subsequent to the viral attack. “And the bacteria that were responsible for those deaths were not drug-resistant because the pandemic occurred before the development of antibiotics,” Riley said. “That wouldn’t be the case today. It’s very likely any highly virulent influenza pandemic would involve a wave of secondary bacterial pneumonia. And that means multi-drug-resistant bacteria would most certainly be involved. To put it mildly, that would be a tremendous challenge for the public health system.”

According to Vance, AIDS patients are highly susceptible to TB. If multi-drug-resistant TB established a beachhead in the United States, our AIDS-affected population would face far more complicated and expensive health care at best, and sharply elevated death rates at worse.

More generally, Reingold observed, relative risk must always be considered when evaluating a microorganism with pandemic potential. “That’s extremely important, in that it allows you to develop appropriate strategies and properly deploy your resources,” he said. “In regard to the risk assessment of future pandemics, we can assume a couple of things. First, we will have them, especially where influenza is concerned. And we will see the emergence of new infectious agents, mainly viruses of [zoonotic origin]. What about severity, time frame, and so forth? Here’s where the great uncertainties lie. If you say you have the answers, you’re delusional. We know there will be pandemics. We don’t know when and how.”

Such uncertainty, of course, is unsettling. So are the limits that time, geography, and resources enforce on any pandemic response. Influenza remains particularly troublesome. Because epidemiologists can’t predict influenza strains, and some strains can change very rapidly, Reingold said, a universal vaccine remains out of reach. And when an identifiable strain does emerge, it can take up to two years to produce enough of the proper vaccine to inoculate global populations. “Meanwhile, it generally takes about two months for influenza to spread around the world,” he said.

Further, reduced funding for public health could greatly limit our response to pandemic, Reingold said. “Despite major investments in the past, basic disease surveillance capabilities and infrastructure have been allowed to decline in the U.S. and the world,” he said. “The critical thing in controlling an infectious disease is local response, whether it’s the Napa Valley or the Congo. You have to be able to detect it and respond quickly. And that front line capability is not in great shape. These days, public health funding in the U.S. is largely a state matter, and the states have found it easy to cut public health budgets. After all, there are no bodies in the street—yet.”

“The biggest en­emy we face in any crisis is deni­al and anxi­ety. We live in a highly com­plex world—really, a messy world—and we can be sure that the com­plex­ity will only in­crease, and that our crises will be lar­ger, they will come at us faster, and they will cost us more money.”

But we also have to recognize the limits of our capabilities. Neither wishful thinking nor panic is productive, observed Ian Mitroff, the senior investigator for Berkeley’s Center for Catastrophic Risk Management and founder of Mitroff Crisis Management consulting firm.

“The biggest enemy we face in any crisis is denial and anxiety,” said Mitroff. “We live in a highly complex world—really, a messy world—and we can be sure that the complexity will only increase, and that our crises will be larger, they will come at us faster, and they will cost us more money. With pandemics, for example, we can’t just consider microbes. We have to consider transportation, local and regional infrastructure and resources, media impacts.”

Mitroff’s view is that there are few natural disasters. Almost all crises, he maintains, are induced and sustained by human beings. A bridge fails not because of an act of God or nature’s fury; it fails because the engineering specs didn’t adequately address adjacent earthquake faults or the impacts of strong currents and tides on the abutments. Similarly, highly lethal influenza variants don’t appear spontaneously. They are created by human beings and livestock living in close proximity, giving flu viruses ample opportunity for gene swapping. Ebola outbreaks are driven by human beings selling and consuming bush meat, and coming into close contact with victims, either living or dead.

“You inevitably arrive at human causes when you follow the chains of events,” says Mitroff. “We have to deal with active crises as best we can, and there’s definitely room for improvement there. But with pandemics, there are so many variables, and they’re always shifting. So we should also try to develop a safety culture, so we can—maybe—prevent some of the crises. We might be able to avoid some outbreaks if we could modify the behaviors and the circumstances that lead to them.”

That could range from increased surveillance at airports and encouraging people to wear face masks during disease outbreaks to regulating livestock production in rural Asia. And that in turn highlights the limitations of any attempt to change the social—and microbiological—status quo. Convincing an educated and sophisticated resident of Kuala Lumpur to wear a face mask is one thing. But convincing a poor and illiterate farmer in a remote Laotian province to forgo raising ducks and pigs in adjacent pens is another: Centuries of tradition and an innate resistance to central authority militate against it.

“We’re grappling with very complex situations, and most people think our job is to come up with a single, effective model with the all the truth wrapped up in it,” says Mitroff. “But most models are simplistic. You don’t need one model. You need many models. In any crisis, you can be sure of one thing—all sacred assumptions will be trashed.” 

Glen Martin is a frequent contributor to California and California Online. His 2012 book, Game Changer: Animal Rights and the Fate of Africa’s Wildlife, was published by UC Press.

From the Summer 2014 Apocalypse issue of California.

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